Transmembrane action potentials were recorded from embryonic rat hearts at ages between 10& days of gestation and birth (21 to 22 days). The resting potential averaged 30 to 40 mv at IOJ2 days and increased to around 80 mv by birth. Two periods of rapid increase in resting potential were noted: 1) from 10^ to 13& days and 2) from 19M days of gestation to birth. The maximal upstroke velocity of the action potential increased as the resting potential increased. The duration of the ventricular and atrial action potentials was inversely related to heart rate, and their rate sensitivity decreased with age. The atrial action potential lost its rate sensitivity by 13M days of gestation and the ventricular action potential lost its by birth. At IOJ2 days diastolic depolarization was found in the area of the ventricle proximate to the A-V junction, the left and right atria, and the sinus venosus. The velocity of the diastolic depolarization was greatest in the sinus venosus and least in the ventricle. The diastolic depolarization decreased with growth and was lost by 13/2 days of gestation. ADDITIONAL KEY WORDScardiac action potentials cardiac pacemaker cardiac electrophysiology diastolic depolarization mammalian embryonic heart growth and differentiation• The transmembrane action potential of the embryonic and fetal heart has been studied principally in the chick embryo (1-7).In the ventricle of 6-to 8-day chick embryo hearts, Lehmkuhl and Sperelalcis (2) found resting potentials of 72 mv and action potentials of 86 mv. Potentials in the range of 30 to 50 mv were found in 37-to 67-hour chick embryos by Meda and Ferroni (3). Action potential configuration was found to be simi-

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The cholinergic innervation of the rabbit heart was studied in vitro and in vivo. An isolated preparation, which included the combined atria, S-A node, A-V node and bundle of His, was mounted so that microelectrodes could be placed in either the specialized or nonspecialized tissues. Using a roving monopolar electrode, local transmural electrical stimulation of intracardiac nerves (nerve stimulation) was applied at the A-V or the S-A node. At the A-V node it induced hyperpolarization, reduced the duration and amplitude of action potentials recorded from three regions of die A-V node and the His bundle, whether the preparation was spontaneously beating or electrically driven in either the forward or retrograde direction, and blocked membrane excitation in the nodal and nodal-His regions and to downstream structures. The depressant effects of nerve stimulation were augmented by physostigmine and antagonized by atropine. Addition of acetylcholine to die bath reduced the frequency at which the A-V node conducted, but in the concentrations used did not duplicate the effects of nerve stimulation. The behavior of the S-A node is qualitatively similar to that of the A-V node. In the presence of a sinus rhythm, nerve stimulation applied at the A-V node did not affect the activity of the S-A node, and during artificial atrial drive, nerve stimulation of the S-A node did not affect A-V nodal function, indicating that little or no neural communication exists between the two regions in die isolated preparation. Locally released acetylcholine appears to depress excitability of specialized cells in the central node, independently of the direction of propagation. ADDITIONAL KEY WORDS transmembrane potentials S-A node cholinergic neurotransmitter innervation in specialized atrial tissues conduction block driving frequency and A-V conduction rabbits• For many years attention has been directed to the influence of A-V nodal conduction on cardiac performance. The introduction of intracellular recording methods has contributed much to the investigation of A-V nodal function. From such studies Hoffman et al.(1-5) proposed that a characteristic feature of the A-V node is the phenomenon of decremental conduction, and emphasized the functional changes which occur in the isolated tissue during rapid atrial excitation combined with the application of acetylcholine. The major change in the A-V node associated with increased frequency of atrial excitation was shown to be a progressive decrease in the rate of depolarization and in the amplitude of nodal action potentials (3). Atrial excitation at a frequency higher than 6.2/sec was not followed by excitation of the A-V node (6). The application of acetylcholine caused marked depression of the amplitude of nodal action potentials during forward, but not retrograde, conduction (2, 5). The observed decrease in the duration and amplitude of atrial action potentials was regarded as an important determinant for the cholinergic block of A-V conduction (5). It was proposed that cholinergic changes in ...

With the aid of electrical stimulation and a combination of acetylcholine and physostigmine, an experimental arrhythmia was predictably induced in isolated atrial segments from rabbits. The tissue was from either left or right atrium, but was not spontaneously active. It was driven electrically at the rate of 2/sec. After the measurement of excitability and of conduction time, both in the presence and absence of ACh, an arrhythmia was induced. The tissue then was divided surgically and the procedure repeated until a residual segment was obtained which did not respond with an arrhythmia. The weight of the nonarrhythmic segment was determined and averaged 32 mg in 16 left atrial preparations, 28 mg in 10 right atrial segments, and 38 mg in 4 segments of left atrium from rabbits chronically treated with reserpine. Calculation of the mean conduction time and of the mean refractory period associated with induction of the experimental arrhythmia indicated that the observed minimal arrhythmic segment was approximately the mass theoretically required if the initiation and maintenance of the arrhythmia were dependent on re-entry excitation.

Ventricular membrane potentials were recorded by the microelectrode technic in anesthetized, open-chest dogs. Concurrently, intraventricular pressure, electrocardiogram and esophageal temperature were recorded. Hypothermia was induced by an extracorporeal cooling method. Data on the parameters observed are presented for a temperature range from 38 to 22 C. The mean temperature for spontaneous ventricular fibrillation was approximately 22 C. Hypothermia increased single fiber action potential duration, primarily by prolonging the plateau phase. Depolarization and terminal repolarization were less affected. Action potential amplitude and resting potential were not changed. Change in action potential duration as a function of varying heart rate became more pronounced with cooling. A characteristic change in action potential shape during early repolarization became evident as hypothermia progressed. Hypothermic changes in the single fiber action potential are compared with changes in the electrocardiogram and the pressure curve. Recordings made from single fibers during hypothermic ventricular fibrillation showed a marked shortening in action potential duration. S ERIOUS disturbances in cardiac function have limited the clinical use of induced hypothermia. Specifically, the greatest hazard is ventricular fibrillation. Hypothermia appears to increase myoeardial vulnerability to stimuli capable of exciting ventricular arrhythmias, for which current therapeutic measures for prevention and control are empirical and generally inadequate.1 ' 2The purpose of this report is to present and to interpret data gathered from experience on dogs in which single cell recording of ventricular membrane potentials was performed in situ. These data are correlated with more conventional parameters of cardiac function. METHODSThirty mongrel dogs of about 10 Kg. weight were used. Pentobarbital sodium was administered in a dose of 30 mg./Kg. intravenously. Following Supported by grants from the Washington State Heart Association and from the Xational Heart Institute, U.S. Public Health Service."Received for publication May 26, 1959. intubation, ventilation of each animal was controlled at a constant rate and volume throughout. The right or left chest was opened through an intercostal incision and the heart was cradled in the pericardium according to conventional technics. A polyethylene catheter was inserted through the wall of the appropriate chamber for the determination of intraventricular pressure by means of a Statham transducer. In some experiments heart rate was artificially altered by electrical stimulation. Bipolar stimulating electrodes were npplied either to the apex or to the right atrium. Stimulating current was supplied by a Tektronix pulse generator assembly. A standard lead II electrocardiogram was obtained, rising needle electrodes. Intracellular recording from either the left or right ventricle was obtained by means of the glass capillary microelectrode adapted for moving tissue. 3 Temperature was monitored from a ther...

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The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.